Caring For The Carer

Seventy-eight percent of employees at Houston hospitals are overweight or obese, according to a study by researchers at The University of Texas Health Science Center at Houston (UTHealth) School of Public Health. The research results were published in the Journal of Occupational and Environmental Medicine.

Employees from six hospitals across Houston, with the exception of physicians, were invited to participate in a survey about their health status and diet in 2012. A total of 924 employees responded to the survey, most of whom classified themselves as hospital administrators or technicians.

“Seventy-eight percent is higher than the national average but not shocking because our study probably attracted employees who wanted to lose weight. Regardless, it is troubling because these are hospital employees active in the workforce and we need them to be healthy. Because obesity is linked to so many cardiometabolic risks, such as elevated glucose and lipids, this calls for immediate intervention to prevent chronic diseases,” said Shreela Sharma, Ph.D., R.D., first author on the paper and associate professor in the Department of Epidemiology, Human Genetics and Environmental Sciences at UTHealth School of Public Health.

According to the results, there was no significant difference in the intake of fruits and vegetables among normal weight, overweight and obese participants, which was generally low across all groups. However, as compared to those of normal weight, obese participants had significantly higher daily consumption of white potatoes such as French fries, regular fat foods (versus reduced or low fat), sugary beverages and added butter and margarine.

Overall, most participants in the study led a sedentary lifestyle. Sixty-five percent of participants reported no days of vigorous physical activity and 48 percent reported no days of moderate physical activity. However, overweight and obese participants spent more time on sedentary behaviours such as watching television. Obese participants also spent more time playing computer games and sitting during the week and on weekends.

“It’s not just about what you don’t do or don’t eat. Behaviours have an additive effect; obesity can happen not just because you didn’t eat enough fruits and vegetables, but because you also ate more fried foods and foods that are higher in fat and not just because you weren’t very active, but also because you were sedentary more often,” said Sharma, who is also a faculty member with the Michael & Susan Dell Center for Healthy Living at the School of Public Health.

Hospital workers are part of a group that suffers from what Sharma calls “the nurturer effect.”

“People who take care of others on a regular basis are generally less likely to take care of themselves. The focus of hospitals is on patient care so sometimes the workers’ own care can take a back seat,” said Sharma.

Nearly 79 percent of survey participants were dissatisfied with their worksite wellness programs and dissatisfaction was highest among obese participants. Given that employees are spending a majority of their waking hours at work, Sharma recommends further investment in worksite-based strategies to promote physical activity and healthy eating, such as healthy vending machine options and accessible walking paths.

“These results highlight the need for hospital employers to better understand, support and nurture the health of their employees,” said Sharma, who added that the local hospitals are interested and invested in employee wellness.

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Everyday Negatives

Flashbacks of scenes from traumatic events often haunt those suffering from psychiatric conditions, such as Post Traumatic Stress Disorder (PTSD). “The close relationship between the human imagery system and our emotions can cause deep emotional perturbations,” says Dr Svetla Velikova of Smartbrain in Norway. “Imagery techniques are often used in cognitive psychotherapy to help patients modify disturbing mental images and overcome negative emotions.” Velikova and her team set out to see if such techniques could become self-guided and developed at home, away from the therapist’s chair.

Healthy people are also emotionally effected by what we see and the images we remember. Velikova explains, “if we visually remember an image from an unpleasant interaction with our boss, this can cause an increased level of anxiety about our work and demotivation.” There is great interest in ways to combat such everyday negative emotional responses through imagery training. But she warns, “this is a challenging task and requires a flexible approach. Each day we face different problems and a therapist teaches us how to identify topics and strategies for imagery exercises.”

To find out if we can train ourselves to use imagery techniques and optimise our emotional state, Velikova and co-workers turned to 30 healthy volunteers. During a two-day workshop the volunteers learnt a series of imagery techniques. They learnt how to cope with negative emotions from past events through imagery transformation, how to use positive imagery for future events or goals, and techniques to improve social interactions and enhance their emotional balance in daily life. They then spent the next 12 weeks training themselves at home for 15-20 minutes a day, before attending another similar two-day workshop.

Velikova compared the results of participant psychological assessment and brain activity, or electroencephalographic (EEG), measurement, before and after the experiment. “The psychological testing showed that depressive symptoms were less prominent. The number of those with sub-threshold depression, expressing depressive symptoms but not meeting the criteria for depression, was halved. Overall, volunteers were more satisfied with life and perceived themselves as more efficient” she explains.

Following analysis, the EEG data showed significant changes in the beta activity in the right medial pre-frontal cortex of the brain. Velikova notes that this region is known to be involved in imaging pleasant emotions and contributing to the degree of satisfaction with life. There were also changes in the functional connectivity of the brain, including increased connectivity between the temporal regions from both hemispheres, which Velikova attributes to enhanced coordination of networks linked to processing of images. She concludes, “this combination of EEG findings also suggests a possible increase in the activity of GABA (gamma-aminobutyric acid), well known for its anti-anxiety and antidepressant properties.”

Velikova and co-workers’ results indicate that self-guided emotional imagery training has great potential to improve the everyday emotional wellbeing in healthy people. The team is now further exploring how the approach affects the cognitive function of healthy people. With minimal professional intervention, this technique could be developed to be a cost-effective aid for those with sub-threshold depression. It could also be promoted by businesses to help improve workforce morale and drive up productivity.

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Going Gluten Free

Unintended Consequences.

People who eat a gluten-free diet may be at risk for increased exposure to arsenic and mercury, toxic metals that can lead to cardiovascular disease, cancer and neurological effects, according to a report in the journal Epidemiology.

Gluten-free diets have become popular in the U.S., although less than 1 percent of Americans have been diagnosed with celiac disease; an out-of-control immune response to gluten, a protein found in wheat, rye and barley.

A gluten-free diet is recommended for people with celiac disease, but others often say they prefer eating gluten-free because it reduces inflammation, a claim that has not been scientifically proven. In 2015, one-quarter of Americans reported eating gluten-free, a 67 percent increase from 2013.

Gluten-free products often contain rice flour as a substitute for wheat. Rice is known to bio-accumulate certain toxic metals, including arsenic and mercury from fertilizers, soil, or water, but little is known about the health effects of diets high in rice content.

Maria Argos, assistant professor of epidemiology in the UIC School of Public Health, and her colleagues looked at data from the National Health and Nutrition Examination Survey searching for a link between gluten-free diet and biomarkers of toxic metals in blood and urine.

They found 73 participants who reported eating a gluten-free diet among the 7,471 who completed the survey, between 2009 and 2014. Participants ranged in age from 6 to 80 years old.

People who reported eating gluten-free had higher concentrations of arsenic in their urine, and mercury in their blood, than those who did not. The arsenic levels were almost twice as high for people eating a gluten-free diet, and mercury levels were 70 percent higher.

“These results indicate that there could be unintended consequences of eating a gluten-free diet,” Argos said. “But until we perform the studies to determine if there are corresponding health consequences that could be related to higher levels of exposure to arsenic and mercury by eating gluten-free, more research is needed before we can determine whether this diet poses a significant health risk.”

“In Europe, there are regulations for food-based arsenic exposure, and perhaps that is something we here in the United States need to consider,” Argos said. “We regulate levels of arsenic in water, but if rice flour consumption increases the risk for exposure to arsenic, it would make sense to regulate the metal in foods as well.”

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Feed A Cold Feed A Fever

When you have a stomach bug, you probably don’t feel much like eating. This loss of appetite is part of your body’s normal response to an illness but is not well understood. Sometimes eating less during illness promotes a faster recovery, but other times, such as when cancer patients experience wasting, the loss of appetite can be deadly.

Now, research from the Salk Institute shows how bacteria block the appetite loss response in their host to both make the host healthier and also promote the bacteria’s transmission to other hosts. This surprising discovery, published in the journal Cell, reveals a link between appetite and infection and could have implications in treating infectious diseases, infection transmission and appetite loss associated with illness, aging, inflammation or medical interventions (like chemotherapy).

“It’s long been known that infections cause loss of appetite but the function of that, if any, is only beginning to be understood,” says Janelle Ayres, assistant professor at Salk Institute’s Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis.

Mice orally infected with the bacteria Salmonella Typhimurium typically experience appetite loss and eventually become much sicker as the bacteria become more virulent, spreading from the intestines to other tissues in the body. Ayres’ team tested different conditions in the infected mice and found that sick mice that consumed extra calories despite their appetite loss actually survived longer. It turns out this survival wasn’t due to a more active immune response by well-fed animals (as measured by levels of the bacteria in the host). Instead, it was because the Salmonella weren’t spreading outside of the intestines and throughout the body when the mice ate more, which enabled the animals to stay healthy despite infection. Even more surprising, the Salmonella were acting on the intestine to try to suppress the appetite loss in the host.

The finding was initially puzzling: why would the bacteria become less virulent and not spread to other areas in the body when nutrients were more plentiful? And why would Salmonella actively promote this condition? It turns out the bacteria were making a tradeoff between virulence, which is the ability of a microbe to cause disease within one host and transmission, which is its ability to spread and establish infections between multiple hosts.

“What we found was that appetite loss makes the Salmonella more virulent, perhaps because it needs to go beyond the intestines to find nutrients for itself. This increased virulence kills its host too fast, which compromises the bacteria’s ability to spread to new hosts,” explains Sheila Rao, a Salk research associate and the first author on the study. “The tradeoff between transmission and virulence has not been appreciated before; it was previously thought that virulence and transmission were coupled.”

When the host ate more and survived longer during infection, the Salmonella benefitted: bacteria in those mice were able to spread via faeces to other animals and increase its transmission between hosts, as compared to bacteria in mice who didn’t eat and died sooner due to heightened bacterial virulence.

The researchers discovered that, to halt the appetite-loss response and boost transmission between hosts, Salmonella produces a molecule called SlrP, which blocks activation of an immune protein (cytokine) in the intestines. This cytokine typically communicates with the brain’s appetite centre, called the hypothalamus, to prompt the host to lose its appetite during infection. The team found that mice infected with Salmonella that couldn’t make SlrP ate less food while infected, lost more weight and died faster than control mice.

Though the same gut-brain pathway tied to appetite loss exists in the human as in mice, Ayres cautions that infection responses are dependent on many factors and that whether eating or fasting during illness can improve one’s health will depend in large part on what the causative agent of the infection is. Her team is planning to search the human microbiome (the collection of bacteria that live in people’s bodies) to find other microbes that might have a similar effect on this pathway and explore those for new therapies tied to appetite loss and treating disease. The lab also wants to investigate whether drugs could be used to turn up or down the sickness-induced appetite-loss pathway that SlrP targets.

“Now that we’d identified this mechanism that regulates appetite, we want to turn it on the flip side and see if we can decrease appetite via this mechanism to help in cases of metabolic disease,” says Ayres.

The discovery also points to the tantalising possibility of treating infectious diseases with approaches other than antibiotics, such as nutritional intervention. “Finding alternatives to antibiotics is incredibly important as these drugs have already encouraged the evolution of deadly antibiotic-resistant strains,” says Ayres. In the United States alone, two million people annually become infected with bacteria that are resistant to antibiotics and at least 23,000 people die each year as a direct result of these infections, according to the U.S. Centers for Disease Control.

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Licenced To Kill

Smoking related imagery is conspicuous by its absence from only one Bond movie since 007 first graced cinema screens in 1962, finds an analysis in Tobacco Control.

And while Bond himself has stubbed out his last cigarette, with no smoking after 2002, he continues to be exposed to second-hand smoke, including from his sexual partners, the findings show.

Given the links between smoking in movies and teens taking it up, and that the James Bond series of movies is the longest running and highest ever grossing movie franchise globally, these findings are of concern, say the researchers.

While several studies have delved into various aspects of Bond’s lifestyle, there hasn’t been any detailed consideration of smoking related content and its potential health impact since the spy first lit up in 1962.

The researchers therefore analysed these themes in the 24 Bond movies screened by Eon Productions, from 1962 (Dr No) up to the latest, Spectre, in 2015.

They found that Bond’s on screen smoking peaked during the 1960s, when he puffed away in 83% of the movies produced in that decade, after which it declined until he took his last puff in 2002 (Die Another Day).

When he was a smoker, he lit up, on average, within 20 minutes of the start of the film.

While smoking has declined among Bond’s sexual partners over the decades, it is still happening, as seen most recently in 2012 in Skyfall.

Smoking by his sexual partners would have exposed Bond to considerable levels of second- hand cigarette smoke, although the typically brief nature of his romantic liaisons would have at least curbed some of the impact, suggest the researchers.

Smoking related spy gadgetry had a relatively short lifespan in Bond movies, peaking in the 1970s in 80% of the films produced during that decade, but never to be seen again after 1989.

And cigarette branding featured in two movies: in 1979 (Marlboro in Moonraker); and in 1989 (Lark in License to Kill), as part of a product placement deal with Philip Morris to open up the Japanese cigarette market.

Overall, smoking related imagery was absent in only one movie in 2006 (Casino Royale). In the most recent movie, in 2015, none of Bond’s major associates smoked, but other characters still did, adding up to an estimated 261 million ‘tobacco impressions’ for 10-29 year olds in the USA alone.

The researchers note that there have been attempts in the Bond series to mention/depict the hazards of smoking, the first of which came in 1967 (You Only Live Twice), with subsequent references made in 1974, 1979, 1997. And in 1999, Miss Moneypenny hurls Bond’s gift to her of a cigar into the bin in disgust (The World Is Not Enough).

But while there have been some “favourable downward smoking related trends in this movie series, the persisting smoking content remains problematic from a public health perspective, especially given the popularity of the series,” write the researchers.

And they suggest that while smoking seems to be at odds with Bond’s need for physical fitness and his level of educational attainment, it does fit with his disregard for other risks to his health.

After all, 007 has dodged thousands of bullets, he drinks a lot of alcohol, and often drives very fast, they point out. And that’s without a goodly proportion of his sexual partners (nine out of 60) attempting to disable, capture, or kill him.

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What Goes In

Scientists have developed a urine test that measures the health of a person’s diet.

The five-minute test measures biological markers in urine created by the breakdown of foods such as red meat, chicken, fish and fruit and vegetables.

The analysis, developed by researchers from Imperial College London, Newcastle University and Aberystwyth University, also gives an indication of how much fat, sugar, fibre and protein a person has eaten.

Although the work is at an early stage, the team hope that with future development the test will be able to track patients’ diets. It could even be used in weight loss programmes to monitor food intake.

Evidence suggests people inaccurately record their own diets, and under-report unhealthy food while over-reporting fruit and vegetable intake and that the likelihood of inaccuracies in food diaries increases if a person is overweight or obese.

Professor Gary Frost, senior author of the study from the Department of Medicine at Imperial said: “A major weakness in all nutrition and diet studies is that we have no true measure of what people eat. We rely solely on people keeping logs of their daily diets, but studies suggest around 60 per cent of people misreport what they eat to some extent. This test could be the first independent indicator of the quality of a person’s diet and what they are really eating.”

In the study, published in the journal Lancet Diabetes and Endocrinology and conducted at the MRC-NIHR National Phenome Centre, the researchers asked 19 volunteers to follow four different diets, ranging from very healthy to very unhealthy. These were formulated using World Health Organisation dietary guidelines, which advise on the best diets to prevent conditions such as obesity, diabetes and heart disease.

The volunteers strictly followed these diets for three days while in a London research facility, throughout which the scientists collected urine samples in the morning, afternoon and evening.

The research team then assessed the urine for hundreds of compounds, called metabolites, produced when certain foods are broken down in the body.

These included compounds that indicate red meat, chicken, fish, fruit and vegetables, as well as giving a picture of the amount of protein, fat, fibre and sugar eaten. They also included compounds that point to specific foods such as citrus fruits, grapes and green leafy vegetables.

From this information the researchers were able to develop a urine metabolite profile that indicated a healthy, balanced diet with a good intake of fruit and vegetables. The idea is this ‘healthy diet’ profile could be compared to the diet profile from an individual’s urine, to provide an instant indicator of whether they are eating healthily.

The scientists then tested the accuracy of the test on data from a previous study. This included 225 UK volunteers as well as 66 people from Denmark. All of the volunteers had provided urine samples, and kept information on their daily diets.

Analysis of these urine samples enabled the researchers in the current study to accurately predict the diet of the 291 volunteers.

Professor John Mathers, co-author from the Human Nutrition Research Centre at Newcastle University, said: “For the first time, this research offers an objective way of assessing the overall healthiness of people’s diets without all the hassles, biases and errors of recording what they’ve eaten.”

The team now hope to refine the technology by testing it on larger numbers of people. They also need to further assess the accuracy of the test on an average person’s diet, outside of a research setting.

Dr Isabel Garcia-Perez, co-author from the Faculty of Medicine at Imperial explained: “We need to develop the test further so we can monitor the diet based on a single urine sample, as well as increase the sensitivity. This will eventually provide a tool for personalised dietary monitoring to help maintain a healthy lifestyle. We’re not at the stage yet where the test can tell us a person ate 15 chips yesterday and two sausages, but it’s on the way.”

The team added the technology may one day be used alongside weight loss programmes, as well as patient rehabilitation, for instance to help heart attack patients follow a healthy diet.

Professor Elaine Holmes, co-author from the Department of Surgery and Cancer at Imperial added: “We are hoping to make this test available to the public within the next two years. The idea would be to collect a urine sample at home and deliver it to a local centre for analysis. We envisage the tool being used by dieticians to help guide their patients’ dietary needs, or even by individuals who are interested in finding out more about the relationship between diet and their health”

Dr Des Walsh, head of population and systems medicine at the Medical Research Council said: “Though this research is still in its early stages, it’s grappling with essential methods in food and diet studies where advances are really needed. Measuring what we eat and drink more accurately will widen the benefits of nutrition research, developing better evidence-based interventions to improve individual’s health and reduce obesity.”

Professor John Draper, co-author from Aberystwyth University added: “The future challenge is to apply the technology developed in this laboratory study in a community setting and objectively monitor diet in the home. The teams in Aberystwyth and Newcastle have been doing just this and the results are looking very promising.”

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Scleroderma And Melanoma

Michigan State University researchers have discovered that a chemical compound, and potential new drug, reduces the spread of melanoma cells by up to 90 percent.

The human-made, small-molecule drug compound goes after a gene’s ability to produce RNA molecules and certain proteins in melanoma tumours. This gene activity, or transcription process, causes the disease to spread but the compound can shut it down. Up until now, few other compounds of this kind have been able to accomplish this.

“It’s been a challenge developing small-molecule drugs that can block this gene activity that works as a signaling mechanism known to be important in melanoma progression,” said Richard Neubig, a pharmacology professor and co-author of the study. “Our chemical compound is actually the same one that we’ve been working on to potentially treat the disease scleroderma, which now we’ve found works effectively on this type of cancer.”

Scleroderma is a rare and often fatal autoimmune disease that causes the hardening of skin tissue, as well as organs such as the lungs, heart and kidneys. The same mechanisms that produce fibrosis, or skin thickening, in scleroderma also contribute to the spread of cancer.

Small-molecule drugs make up over 90 percent of the drugs on the market today and Neubig’s co-author Kate Appleton, a postdoctoral student, said the findings are an early discovery that could be highly effective in battling the deadly skin cancer. It’s estimated about 10,000 people die each year from the disease.

Their findings are published in  Molecular Cancer Therapeutics.

“Melanoma is the most dangerous form of skin cancer with around 76,000 new cases a year in the United States,” Appleton said. “One reason the disease is so fatal is that it can spread throughout the body very quickly and attack distant organs such as the brain and lungs.”

Through their research, Neubig and Appleton, along with their collaborators, found that the compounds were able to stop proteins, known as Myocardin-related transcription factors, or MRTFs, from initiating the gene transcription process in melanoma cells. These triggering proteins are initially turned on by another protein called RhoC, or Ras homology C, which is found in a signaling pathway that can cause the disease to aggressively spread in the body.

The compound reduced the migration of melanoma cells by 85 to 90 percent. The team also discovered that the potential drug greatly reduced tumours specifically in the lungs of mice that had been injected with human melanoma cells.

“We used intact melanoma cells to screen for our chemical inhibitors,” Neubig said. “This allowed us to find compounds that could block anywhere along this RhoC pathway.”

Being able to block along this entire path allowed the researchers to find the MRTF signaling protein as a new target.

Appleton said figuring out which patients have this pathway turned on is an important next step in the development of their compound because it would help them determine which patients would benefit the most.

“The effect of our compounds on turning off this melanoma cell growth and progression is much stronger when the pathway is activated,” she said. “We could look for the activation of the MRTF proteins as a biomarker to determine risk, especially for those in early-stage melanoma.”

According to Neubig, if the disease is caught early, chance of death is only 2 percent. If caught late, that figure rises to 84 percent.

“The majority of people die from melanoma because of the disease spreading,” he said. “Our compounds can block cancer migration and potentially increase patient survival.”

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